2021
DOI: 10.1152/jn.00348.2020
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Spinal cord fractalkine (CX3CL1) signaling is critical for neuronal sensitization in experimental nonspecific, myofascial low back pain

Abstract: Neuroactive substances released by activated microglia contribute to hyperexcitability of spinal dorsal horn neurons in many animal models of chronic pain. An important feedback loop mechanism is via release of fractalkine (CX3CL1) from primary afferent terminals and dorsal horn neurons and binding to CX3CR1 receptors on microglial cells. We studied the involvement of fractalkine signaling in latent and manifest spinal sensitization induced by two injections of nerve growth factor (NGF) into the lumbar multifi… Show more

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Cited by 19 publications
(16 citation statements)
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“…CX3CL1 (also called fractalkine), the only member of the C-X3-C group, is constitutively expressed in the neurons of the normal peripheral nervous system and the central nervous system [ 68 , 69 ]. Chemokine pairs CX3CL1/CX3CR1 are involved in neuropathic pain via neuron-microglia interaction in the spinal cord [ 70 72 ]. P38, a member of mitogen-activated protein kinases (MAPKs), is an important downstream kinase of CX3CL1/CX3CR1 signaling [ 73 75 ].…”
Section: Discussionmentioning
confidence: 99%
“…CX3CL1 (also called fractalkine), the only member of the C-X3-C group, is constitutively expressed in the neurons of the normal peripheral nervous system and the central nervous system [ 68 , 69 ]. Chemokine pairs CX3CL1/CX3CR1 are involved in neuropathic pain via neuron-microglia interaction in the spinal cord [ 70 72 ]. P38, a member of mitogen-activated protein kinases (MAPKs), is an important downstream kinase of CX3CL1/CX3CR1 signaling [ 73 75 ].…”
Section: Discussionmentioning
confidence: 99%
“…Thermal hyperalgesia and mechanical allodynia can also be elicited in naïve animals by an intrathecal injection of FKN ( 44 ) and both effects are abrogated in CX 3 CR 1 knockout mice ( 34 , 45 ). In addition, the administration of a neutralizing antibody against CX 3 CR 1 ( 46 , 47 ) reduces pain-like behaviours in neuropathic pain models, indicating that microglia-mediated mechanisms contribute to nociceptive hypersensitivity. Injection of FKN, after unique binding to CX 3 CR 1 , activates p38 MAPK signalling pathway ( 34 ).…”
Section: Introductionmentioning
confidence: 99%
“…The time delay and magnitude of the contralateral sensitivity also aligns well with the process being dependent on an immune-related and/or diffusion process. In male rats, the early stages of pain development, wherein primary afferent priming via NGF exposure leads to spinal neuronal sensitization in this unilateral NGF-LBP model, depend initially on microglial activation and are maintained by astrocyte activation [ 29 , 54 ]. Additional work on the presence, level, and mechanisms of immune cell activation throughout the spinal cord in male and female rodents should be considered [ 7 ].…”
Section: Discussionmentioning
confidence: 99%